We postulate that a chronically established thymic inflammation may be essential, in the context of a genetically predisposing background, for the establishment of mechanisms contributing to MG autoimmunity including presentation of “self-epitopes”; upregulation of MHC genes, of type I IFNs, of proinflammatory cytokines, of adhesion, and of costimulatory molecules on antigen-presenting cells; as well as the constant priming of autoreactive T cells [13] (Figure 7). This evidence concerns the gene CD276 and myasthenia gravis.